• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

Beta-amyloid protein increases the vulnerability of cultured cortical neurons to excitotoxic damage.

作者信息

Koh J Y, Yang L L, Cotman C W

机构信息

Department of Psychobiology, University of California, Irvine 92717.

出版信息

Brain Res. 1990 Nov 19;533(2):315-20. doi: 10.1016/0006-8993(90)91355-k.

DOI:10.1016/0006-8993(90)91355-k
PMID:2289145
Abstract

Glutamate neurotoxicity may be an underlying pathological mechanism contributing to neuronal cell loss in a variety of conditions including Alzheimer's disease (AD). In this study, we examined whether the beta-amyloid protein found in the neuritic plaques of AD alters the susceptibility of neurons to excitotoxic damage. While mature cortical neurons exposed to beta-amyloid protein for 2-4 days did not appear to be damaged, their vulnerability to low-intensity exposure to glutamate, N-methyl-D-aspartate, and kainate increased, suggesting that this mechanism may contribute to the neurodegeneration seen in AD.

摘要

相似文献

1
Beta-amyloid protein increases the vulnerability of cultured cortical neurons to excitotoxic damage.
Brain Res. 1990 Nov 19;533(2):315-20. doi: 10.1016/0006-8993(90)91355-k.
2
Cortical neurons containing somatostatin- or parvalbumin-like immunoreactivity are atypically vulnerable to excitotoxic injury in vitro.含有生长抑素样或小白蛋白样免疫反应性的皮质神经元在体外对兴奋性毒性损伤异常敏感。
Neurology. 1990 Aug;40(8):1288-92. doi: 10.1212/wnl.40.8.1288.
3
Parallel development of excitotoxic vulnerability to N-methyl-D-aspartate and kainate in dispersed cultures of the rat cerebral cortex.大鼠大脑皮层分散培养物中对N-甲基-D-天冬氨酸和红藻氨酸的兴奋性毒性易感性的平行发展。
Neuroscience. 1991;43(1):35-40. doi: 10.1016/0306-4522(91)90414-j.
4
Beta-amyloid increases neuronal susceptibility to injury by glucose deprivation.β-淀粉样蛋白会增加神经元对葡萄糖剥夺损伤的易感性。
Neuroreport. 1991 Dec;2(12):763-5. doi: 10.1097/00001756-199112000-00008.
5
Lack of excitotoxic cell death in serum-free cultures of rat cerebral cortex.
Brain Res. 1990 Sep 3;526(2):328-32. doi: 10.1016/0006-8993(90)91241-8.
6
A metabotropic glutamate receptor agonist does not mediate neuronal degeneration in cortical culture.代谢型谷氨酸受体激动剂不会介导皮质培养物中的神经元变性。
Brain Res. 1991 Oct 11;561(2):338-43. doi: 10.1016/0006-8993(91)91613-6.
7
GABA does not protect cerebro-cortical cultures against excitotoxic cell death.γ-氨基丁酸不能保护大脑皮质培养物免受兴奋性毒性细胞死亡的影响。
Eur J Pharmacol. 1990 Jun 21;182(1):203-6. doi: 10.1016/0014-2999(90)90515-8.
8
Neurodegeneration mediated by glutamate and beta-amyloid peptide: a comparison and possible interaction.由谷氨酸和β-淀粉样肽介导的神经退行性变:比较与可能的相互作用
Brain Res. 1995 Sep 11;691(1-2):169-79. doi: 10.1016/0006-8993(95)00669-h.
9
Comparison of double fluorescence staining and LDH-test for monitoring cell viability in vitro.
Neuroreport. 1993 Nov 18;5(2):129-32. doi: 10.1097/00001756-199311180-00008.
10
Insulin-specific sensitization of cultured cerebrocortical neurons to glutamate excitotoxicity.培养的大脑皮质神经元对谷氨酸兴奋性毒性的胰岛素特异性致敏作用。
Brain Res. 1992 May 15;580(1-2):331-3. doi: 10.1016/0006-8993(92)90962-9.

引用本文的文献

1
Cerebrovascular Dysfunction in Alzheimer's Disease and Transgenic Rodent Models.阿尔茨海默病及转基因啮齿动物模型中的脑血管功能障碍
J Exp Neurol. 2024;5(2):42-64. doi: 10.33696/neurol.5.087.
2
The Novel Role of Mitochondrial Citrate Synthase and Citrate in the Pathophysiology of Alzheimer's Disease.线粒体柠檬酸合酶及其代谢产物柠檬酸在阿尔茨海默病发病机制中的新作用。
J Alzheimers Dis. 2023;94(s1):S453-S472. doi: 10.3233/JAD-220514.
3
Mitochondrial SIRT3 Deficiency Results in Neuronal Network Hyperexcitability, Accelerates Age-Related Aβ Pathology, and Renders Neurons Vulnerable to Aβ Toxicity.
线粒体 SIRT3 缺乏导致神经元网络过度兴奋,加速与年龄相关的 Aβ 病理学,并使神经元易受 Aβ 毒性影响。
Neuromolecular Med. 2023 Mar;25(1):27-39. doi: 10.1007/s12017-022-08713-2. Epub 2022 Jun 24.
4
Amyloid Beta-Related Alterations to Glutamate Signaling Dynamics During Alzheimer's Disease Progression.淀粉样β相关的谷氨酸信号动力学改变在阿尔茨海默病进展过程中。
ASN Neuro. 2019 Jan-Dec;11:1759091419855541. doi: 10.1177/1759091419855541.
5
BACE1 SUMOylation increases its stability and escalates the protease activity in Alzheimer's disease.BACE1 SUMOylation 增加其稳定性并加剧阿尔茨海默病中的蛋白酶活性。
Proc Natl Acad Sci U S A. 2018 Apr 10;115(15):3954-3959. doi: 10.1073/pnas.1800498115. Epub 2018 Mar 26.
6
Role of Glycogen Synthase Kinase-3β in APP Hyperphosphorylation Induced by NMDA Stimulation in Cortical Neurons.糖原合酶激酶-3β在NMDA刺激诱导的皮质神经元APP过度磷酸化中的作用
Pharmaceuticals (Basel). 2010 Jan 7;3(1):42-58. doi: 10.3390/ph3010042.
7
Heteroreceptor Complexes Formed by Dopamine D, Histamine H, and N-Methyl-D-Aspartate Glutamate Receptors as Targets to Prevent Neuronal Death in Alzheimer's Disease.作为预防阿尔茨海默病神经元死亡的靶点的多巴胺 D、组胺 H 和 N-甲基-D-天冬氨酸谷氨酸受体形成的异源受体复合物。
Mol Neurobiol. 2017 Aug;54(6):4537-4550. doi: 10.1007/s12035-016-9995-y. Epub 2016 Jul 1.
8
Targeting the BACE1 Active Site Flap Leads to a Potent Inhibitor That Elicits Robust Brain Aβ Reduction in Rodents.靶向β-分泌酶1(BACE1)活性位点侧翼可产生一种强效抑制剂,该抑制剂能使啮齿动物大脑中的β淀粉样蛋白(Aβ)显著减少。
ACS Med Chem Lett. 2016 Jan 11;7(3):271-6. doi: 10.1021/acsmedchemlett.5b00432. eCollection 2016 Mar 10.
9
Calpain-Mediated Degradation of Drebrin by Excitotoxicity In vitro and In vivo.钙蛋白酶在体外和体内通过兴奋毒性介导的 drebrin 降解
PLoS One. 2015 Apr 23;10(4):e0125119. doi: 10.1371/journal.pone.0125119. eCollection 2015.
10
Potential natural products for Alzheimer's disease: targeted search using the internal ribosome entry site of tau and amyloid-β precursor protein.用于阿尔茨海默病的潜在天然产物:利用tau蛋白和淀粉样前体蛋白的内部核糖体进入位点进行靶向搜索
Int J Mol Sci. 2015 Apr 20;16(4):8789-810. doi: 10.3390/ijms16048789.